ArticleBMC complementary medicine and therapies2025
Integrating serum pharmacochemistry with network pharmacology and pharmacological validation to elucidate the mechanism of KaiXinSan in treating insomnia.
Article in BMC complementary medicine and therapies, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundKaiXinSan (KXS) is a classic Chinese herbal compound used for treating insomnia and related mental disorders. Modern medical studies have shown that KXS can treat depression, Alzheimer's disease, memory loss, and other conditions. In addition, the effect of KXS in treating insomnia has been confirmed in clinical applications and animal experiments. However, the mechanism by which KXS treats insomnia remains unclear. The purpose of this study is to evaluate the impact of KXS on insomnia and explore its mechanism.
methodsA rat insomnia model was established using p-chlorophenylalanine (PCPA). Pharmacodynamic evaluation was performed via animal behavioral assessments, ELISA detection of biochemical indicators, and pathological tissue observation. The key mechanisms of KXS in treating insomnia were clarified through an integrated approach combining serum pharmacochemistry, network pharmacology, transcriptomics, and metabolomics. These mechanisms were further validated by molecular docking, in vivo, and in vitro experiments.
resultsKXS improved motor activity and sleep status in insomniac rats and alleviated hippocampal neuronal damage. ELISA analysis showed that KXS increased levels of 5-HT and GABA while reducing DA and NE levels in rats. Additionally, KXS decreased levels of TNF-α, IL-6, IL-1β, and ROS. Using UPLC-Q-Orbitrap MS/MS technology, 169 chemical components and 39 blood- enterable components of KXS were identified. Results from network pharmacology and transcriptomics indicated that KXS treats insomnia by regulating serotonin synapse and TNF signaling pathways. Furthermore, KXS reversed abnormal arachidonic acid and tryptophan metabolism in insomniac rats. Molecular docking, immunohistochemistry, and Western blotting showed that active components of KXS exhibited strong binding affinity to relevant proteins, upregulating 5-HTR1A and GABAA protein expression while inhibiting TNF-α and IL-6 protein expression. Cell experiments confirmed that KXS medicated serum reduced LPS induced neuronal damage and inflammatory responses in neural cells.
conclusionsKXS treats insomnia by regulating serotonin synapse signaling pathways and inflammatory responses, and influencing arachidonic acid and tryptophan metabolism.
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